ONEMED FORUM 2013 PRESENTATIONcontent.stockpr.com/amarantus/media/98dab0ebe3381986ef...1. Rodents lesioned with 6-OHDA on one side of their brain at t = 0 2. Behaviour tested for baseline

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Amarantus BioScience, Inc.675 Almanor Ave

Sunnyvale CA 94085OTCQB: AMBS

[email protected]

ONEMED FORUM 2013 PRESENTATION

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SAFE HARBOR

This presentation contains “forward-looking statements” within the meaning ofthe “safe-harbor” provisions of the Private Securities Litigation Reform Act of1995. Such statements involve known and unknown risks, uncertainties and otherfactors that could cause the actual results of the Company to differ materiallyfrom the results expressed or implied by such statements, including changes fromanticipated levels of sales, future international, national or regional economic andcompetitive conditions, changes in relationships with customers, access to capital,difficulties in developing and marketing new products and services, marketingexisting products and services, customer acceptance of existing and new productsand services and other factors. Accordingly, although the Company believes thatthe expectations reflected in such forward looking statements are reasonable,there can be no assurance that such expectations will prove to be correct. TheCompany has no obligation to update the forward-looking information containedin this presentation.

INVESTMENT HIGHLIGHTS

$3B+ Market, growing 8.6% CAGR according to Datamonitor 6M+ Parkinson’s disease (PD) Patients Worldwide Incidence estimated to double by 2032No marketed disease modifying treatments

MANF: Anti-apoptotic Therapeutic Protein PD disease-modifying treatment Other Apoptosis-related applications

Diagnostic Blood Tests NuroPro: PD early-stage diagnostic, other applications LymPro: Alzeimers disease (AD) early-stage diagnostic

Parkinson’sParkinson’s

AmarantusAmarantus

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1. Dopaminergic neuron (DA) cell bodies degenerate in the substantia nigra (SNc)2. SNc degeneration leads to retraction of DA terminals from the Striatum3. Loss of Striatum innervation decreases dopamine, resulting in PD symptoms4. Current approved drugs focus on replacing dopamine in Striatum

Basal Ganglia CircuitSNc

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STRIATUM: BROKEN CIRCUIT IN PD

Results compare GDNF and MANF when 10ug of each wasdelivered to the SNc in neurorestoration rat model of PD.

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STRIATUM REINNERVATION CRITICAL

GDNF MANF

Behavioral Recovery NO YES

Reinnervates Striatum NO YES

Increases dopamine concentrations inStriatum

NO YES

1. Rodents lesioned with 6-OHDA on one side of their brain at t = 02. Behaviour tested for baseline at t = 1 week DA neurons begin to die within 7 days of lesion if left untreated Model mimics later stage PD - fewer DA terminals to control movement

3. Vehicle, MANF (3µg, 10µg or 36µg) or GDNF (10µg) injected at t = 2 weeks4. Behavior tested for drug effect at t = 4 weeks (2 weeks post-treatment)5. Behavior tested for drug effect at t = 6 weeks (4 weeks post-treatment)6. Rats sacrificed at t = 6 weeks to evaluate stereology, densitometry and

neurochemistry analysis

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RAT PD MODEL: 6-OHDA STUDY DESIGN

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Substantia Nigra Stereology Data

VEH 6-OHDA 6-OHDA 6-OHDA 6-OHDA 6-OHDAVEH VEH MANF-3 MANF-10 MANF-36 GDNF-10

DA N

euro

ns/N

igra ±

SEM

(N=6

)

0

5000

10000

15000

20000

25000

30000

35000CONLES

RAT PD MODEL IS PROPERLY CONTROLLED

• This animal model functions properly: Number of DA in the SNc is consistent across untreated and

treated groups (internal control of the model) Model designed to evaluate recovery of remaining injured DA,

thus mimicking later-stage PD

Experiment completed at University of St. Louis Medical School

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-200

-100

0

100

200

300

400

500

600

700

veh/veh 6-ohda/veh 3ug 10ug 36ug GDNF

Tota

l n

et ip

si r

otat

ion

s

Treatment

Restoration

1wkpost…

*

Blue ControlRed 2 Weeks post-treatmentYellow 4 Weeks post treatment

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BEHAVIOR: REDUCE ROTATIONS

MANF significantly reduces behavioral deficitswhereas GDNF does not

N = 12MANF MANF MANF

Experiment completed at UCLA Medical School

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DA PROJECT FROM SNc to SRIATUM

SNc

Striatum

DA Neurons project from the SNc into the Striatum

SNc

Striatum

We measured striatum innervation at 4 locations in striatumat increasing distance away from the SNc

Son

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Tyrosine Hydroxylase Densitometry Data: Striatum

VEH 6-OHDA 6-OHDA 6-OHDA 6-OHDA 6-OHDAVEH VEH MANF-3 MANF-10 MANF-36 GDNF

Den

sito

met

ry U

nits

± S

EM (N

=6)

0

20

40

60

80

100

120CONLES

DENSITOMETRY: DA TERMINALS IN STRIATUM

MANF increases density of DA terminals inStriatum whereas GDNF does not

+14.4% -9.9%

N = 6

Experiment completed at Neuroscience Associates

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DENSITOMETRY: DA TERMINALS IN STRIATUM

CONTROL

6-OHDA

GDNF 10µg

MANF 36µg

MANF 10µg

MANF 3µg

1 2 3 4

Experiment completed at Neuroscience Associates

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NEUROCHEMISTRY: STRIATAL DOPAMINE

Striatal Dopamine

VEH 6-OHDA 6-OHDA 6-OHDA 6-OHDA 6-OHDAVEH VEH MANF-3 MANF-10 MANF-36 GDNF-10

DA

(% U

nles

ione

d C

ontro

l) ±

SEM

(N=2

-6)

0

20

40

60

80

100

120

140

160

MANF increases concentration of dopamine in the striatumwhereas GDNF does not (preliminary evidence)

Experiment completed at PharmaNet (Princeton, NJ)

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MANF: ENCOURAGING DATA FOR PD

MANF1. Reinnervates the striatum2. Produces behavioral recovery3. Increases dopamine concentration in the striatum4. Improves protein folding5. Reduces intracellular calcium

Conclusion: MANF 10µg appears to have the best profile of activity in this model MANF is a potentially promising disease-modifying drug candidate for the

treatment of PD with potential benefits over GDNF

• Breakthrough Biology• Autocrine and paracrine cellular roles• Upregulation / secretion in response to stress• Neurorestoration• Corrects Protein Mis-folding• Regulates Intracellular Calcium• Reduces Apoptosis

• Other Applications:• Cardiovascular Disease• Traumatic Brain Injury• Stroke• Orphan diseases under evaluation

MANF: BEYOND PARKINSON’S

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Lindholm and Saarma, DevNeurobiol (2010)

N-Terminal

C-TerminalProtein folding